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在帕金森氏症的細胞與生物模式中探討PLA2G6及PLA2G6點突變

為了解決2204 PTT的問題，作者劉涵芳 這樣論述：

Table of Contents中文摘要 iAbstract iiTable of Contents iiiList of Figures vList of tables viAbbreviation viiChapter 1. Introduction - 1 -1.1 Phospholipase A2, group VI - 1 -1.2 Parkinson’s disease - 2 -1.3 PLA2G6 and young-onset dystonia-parkinsonism (Parkinson disease-14, P

ARK14) - 3 -1.4 PLA2G6 activity and lipid metabolites - 4 -1.5 Zebrafish as a Model for Neurodegenerative Disorders - 5 -Chapter 2. Materials and Methods - 7 -2.1 Animal Maintenance - 7 -2.2 mRNA preparation and microinjection - 7 -2.3 Zebrafish behavior - 8 -2.4 Histological an

alysis - 8 -2.5 Phospholipase activity assay - 11 -2.6 High performance liquid chromatography (HPLC) - 12 -2.7 Lipophilic metabolites extraction and data processing - 12 -2.8 Mouse behavior - 13 -2.9 Cell culture and Immunocytochemistry - 14 -2.10 Western blot - 15 -2.11 Quantit

ative reverse transcription PCR (qRT-PCR) - 16 -2.12 Statistical analysis - 17 -Chapter 3. Results - 18 -3.1 Characterization of PLA2G6 mutations in zebrafish - 18 -3.1.1 Overexpression of PLA2G6 mutations in zebrafish - 18 -3.1.2 PLA2G6 mutation D331Y and T572I overexpression induced

motility defects in zebrafish - 18 -3.1.3 PLA2G6 mutation D331Y and T572I overexpression caused dopamine neuron loss in zebrafish - 20 -3.2 PLA2G6 phospholipase activity and lipid metabolites - 21 -3.2.1 Zebrafish Pla2g6 is homologous to human PLA2G6 - 21 -3.2.2 PLA2G6 mutation D331Y or

T572I results in decreased phospholipase activity and disturbed lipidome - 22 -3.2.3 Dietary DHA supplementation relieved the motility defects of PLA2G6D331Y/D331Y mice at an early stage of disease onset - 23 -3.3 PLA2G6 in dopaminergic neuron development - 25 -3.3.1 Zebrafish pla2g6 expre

ssed mainly in the central nervous system - 25 -3.3.2 PLA2G6 mutation D331Y or T572I reduced neuronal precursor cells through increased apoptosis - 26 -3.4 The role of PLA2G6 in regulating cellular processes - 27 -3.4.1 Transduction of human wild type PLA2G6 improved proliferation in dopami

nergic neuron cell line - 27 -3.4.2 PLA2G6 play a protective role in dopaminergic neuron cell line under ROS stress - 28 -Chapter 4. Discussion - 29 -4.1 PLA2G6 mutations in PARK14 - 29 -4.2 PLA2G6 mutation and phospholipase activity in PARK14 - 30 -4.3 The role of DHA in PLA2G6 mutat

ion-induced PD - 31 -4.4 PLA2G6-mediated apoptosis in the dopaminergic neuron. - 33 -4.5 PLA2G6 and its metabolites in neurodevelopment. - 34 -4.6 The potential signaling regulation role of PLA2G6 - 36 -Chapter 5. Conclusion - 37 -References - 38 -Figures and Legends - 48 -Table

s - 68 -Publications - 73 -List of FiguresFigure 1. Alignment of PLA2G6 human and zebrafish homologue. - 49 -Figure 2. Schematic illustration of PLA2G6 domains and six point mutations of PARK14. - 50 -Figure 3. Injection of PLA2G6D331Y or PLA2G6T572I causes motility defects in zebrafish.

- 51 -Figure 4. Injection of PLA2G6D331Y or PLA2G6T572I decreases dopaminergic neurons and dopamine levels. - 52 -Figure 5. Injection of PLA2G6D331Y, PLA2G6T572I, or pla2g6 deletion constructs alters phospholipase activity in zebrafish. - 53 -Figure 6. Co-expression of zebrafish pla2g6 res

cues the behavioral defects induced by PLA2G6D331Y or PLA2G6T572I. - 54 -Figure 7. Lipid metabolites are disturbed in PLA2G6D331Y or PLA2G6T572I injected embryos. - 55 -Figure 8. Dietary DHA supplementation does not affect the body weight and diet consumption of PLA2G6 knock-in mice. - 56 -

Figure 9. Dietary DHA supplementation relieves the motility defects of PLA2G6D331Y/D331Y mice at an early stage of disease onset. - 58 -Figure 10. Dietary DHA supplementation does not relieve the motility defects of PLA2G6D331Y/D331Y mice at a late stage of disease onset. - 59 -Figure 11. Zebr

afish pla2g6 is expressed in the developing nervous system. - 60 -Figure 12. Injection of PLA2G6D331Y or PLA2G6T572I reduces the expression of the neuronal precursor marker and induces cell apoptosis. __ - 61 -Figure 13. Injection of PLA2G6D331Y or PLA2G6T572I does not affect the expression of

the neural progenitor marker. - 62 -Figure 14. Expression of human PLA2G6 enhances the proliferation of MN9D cells. - 63 -Figure 15. Expression of hPLA2G6 reduces cell apoptosis upon 6-OHDA treatment in MN9D cells. - 64 -Figure 16. 3D structure predictions of PLA2G6 and the effect of D331Y

or T572I mutation analyzed by PyMOL software. - 65 -Figure 17. Injection of PLA2G6 mutation PLA2G6D331Y or PLA2G6T572I, or pla2g6 deletion constructs pla2g6∆ANK or pla2g6∆Ptt affect the expression of Notch signaling downstream genes. - 66 -Figure 18. The summary of this study. - 67 -List o

f tablesTable 1. List of lipid metabolites identified in PLA2G6D331Y or PLA2G6T572I injected embryos. - 69 -Table 2. Lipid metabolites identified conditions in LC-MS and METLIN database. - 70 -Table 3. Primers used for gene cloning in this thesis. - 71 -Table 4. Primers used for qRT-PCR ana

lysis in this thesis - 72 -

基於倒傳遞神經網絡的雙PPG信號連續血壓預測分析與多指標量測平台之研製

為了解決2204 PTT的問題，作者蔡承洋 這樣論述：

現今社會大多數人因為長期壓力過大缺乏規律的運動，加上飲食習慣的改變大多以重口味食物為主，造成心血管疾病年齡層逐年下降，其中高血壓帶來的併發症最為嚴重，所以提前的預防高血壓與有效監控高血壓疾病患者是將來一項重要的預防項目。論文針對傳統袖帶血壓量測的不連續性與血壓轉換器(Blood Pressure Transducer)的不舒適性，建立一套分析兩個光體積變化描記圖(Photoplethysmography,PPG)結合倒傳遞類神經網路(Back-propagation Neural Network, BP-NN)來完成連續監控非侵入式血壓量測系統。系統除了完成連續血壓預測外，對於心血管關相關參

數，如脈波傳遞時間(Pulse Transmit Time,PTT)、脈波傳遞速度(Pulse Wave Velocity,PWV)、脈波分析(Pulse Waveform Analysis,PWA)、灌流指標(Perfusion Index,PI)以及心率(Heart Rate,HR)也可以同時經由演算法得到，在臨床上也可提供極高的使用價值。本研究採用兩個光體積變化描記圖，利用發光二極體照射皮膚量測血液對光吸收變化量，並利用光反射原理，使用光感測器取得原始反射光訊號，因為脈搏波沿著動脈的長度的傳輸導致血液量的微小增加，檢查動脈上特定點的PPG傳感器可以有效的量測每個心動週期的體積增量，沿著動

脈放置在預定遠端位置的第二個PPG傳感器可以在小延遲之後量測到相同的脈搏波，並從兩個PPG訊號波形上取得與計算血壓相關的特徵訊號，將特徵訊號輸入BP-NN運算，取得估計血壓比對非侵入式血壓(Non-invasive blood pressure,NIBP)，建立準確預防高血壓疾病發生與監控高血壓病患的平台裝置。實驗結果收縮壓(Systolic Blood Pressure,SBP)平均值與標準差為2.23 2.24mmHg，均方差為3.15mmHg；舒張壓(Diastolic blood pressure,DBP)值平均值與標準差為3.5 3.53mmHg，均方差為4.96mmHg。